Common widely used vaccines are made from pathogens (e.g., microorganisms, viruses) or such pathogens whose toxicity is partially weakened or eliminated. The vaccines are administered to living bodies to induce immunity to prevent infectious diseases.
Dendritic cells after having engulfed viruses, microorganisms, or like foreign bodies migrate to lymph nodes and give naive T cells (Th0 cells) the information of the foreign bodies, thus inducing the differentiation of helper T cells. Through the interaction with dendritic cells, Th0 cells differentiate into type 1 helper T cells (Th1 cells), which are responsible for cellular immunity, and type 2 helper T cells (Th2 cells), which are responsible for humoral immunity (see Non-Patent Literature 1, for example).
Many toll-like receptors (TLRs) are expressed in immunocompetent cells responsible for the innate immunity system, including dendritic cells. They are activated upon receiving a TLR ligand and promote the differentiation of helper T cells, thus inducing an effective immune reaction (see Non-Patent Literature 2, for example). For immunity activation, only the reaction routes via TLRs have been known, and other reaction routes have remained unclear.
It is known that the direction of the differentiation of helper T cells is controllable with biological signaling molecules such as cytokines. Such control is widely employed in in vitro testing systems. The dendritic cells are activated by stimuli such as cytokines and assumed to determine the direction of the helper T cell differentiation through complicated signal transduction. That is, the “state” of dendritic cells decides the differentiation of T cells, leading to the induction of the cellular immunity or the humoral immunity. The former, where Th 1 cells serve as the center of the reaction, is called Th1 reaction. Similarly, the latter is called Th2 reaction (see Non-Patent Literature 3, for example).
The promotion of immune reactions via TLRs as described above has been known, but promotion of a humoral immune response (Th2 reaction) via other reactions, that is, reactions not involving TLR stimuli by TLR ligands, has yet to be reported.
It is known that immunity activation effects can be given by toxins such as cholera toxin or Escherichia coli heat-labile enterotoxin or fat/oil adjuvants that enhance the effects of immune reactions by slow-release of antigens. However, they have problems in terms of the balance between the safety and the efficacy (see Non-Patent Literature 4, for example). Thus, adjuvants capable of activating immunity while ensuring safety are demanded.